Pain variant (status anginosus)
Pain is one of the main symptoms of developing myocardial infarction. Pain variant is observed in 70-95% of patients in acute period of myocardial infarction. The severity of the pain syndrome can fluctuate from unbearable pains to comparatively small pain sensations. But in any case, the pain syndrome with myocardial infarction is superior in strength and duration to the usual pain for the patient, accompanying the attack of angina pectoris. The pain is usually pressing, liquefying, burning, cutting. Sublingual administration of nitroglycerin and other antianginal drugs is ineffective. Even the introduction of narcotic analgesics often gives an incomplete and short-lived effect.
Most often, the pain is localized behind the sternum, in the region of the heart, in the epigastric region. Pain can radiate to the left arm, left shoulder, scapula, neck, interscapular space. The literature describes the symptoms of myocardial infarction with irradiation of pain in the right arm, shoulder, both hands, lower jaw, legs.
The duration of pain ranges from 10-20 minutes to 1 -2 days. It can stop for several hours, and then resume.
Patients are more often restless, groaning, unable to stay in one pose. Pain syndrome in patients with myocardial infarction can be accompanied by a sense of fear, a fear of death. Sometimes the pain becomes unbearable and refractory to drug therapy from the very beginning. Such cases are most often complicated by cardiogenic shock.
There is a definite correlation between the severity of anginal status, the magnitude of myocardial necrosis and its localization. Large focal extensive infarctions, as a rule, are accompanied by an intense pain syndrome. The pain attack with small focal infarction is most often less pronounced.
The syndrome of intense anginal pain basically corresponds to the classical description of anginal status. It is caused by acute myocardial ischemia. With the onset of necrosis, as a rule, the symptoms of myocardial infarction and pain cease, and in the clinical picture of the disease, the signs of a resorptive necrotic syndrome are the first.
Residual pains are dull aching in nature, do not cause disturbances in well-being and the condition of patients.
Pericardial pains usually stitching, are felt on deep inspiration and when the position of the body changes, are associated with the involvement of the pericardium in the inflammatory process.
With an atypical pain syndrome, the pain is felt only in the areas of irradiation - pain only in the right or left arm, the lower jaw, and so on.
At physical examination in patients with uncomplicated course of myocardial infarction in the first hours after the development of pain syndrome, paleness, cyanosis of the lips, and increased moisture of the skin are revealed. As a rule, pain syndrome is accompanied by the development of tachycardia (up to 100-120 beats / min), rarely bradycardia. Subsequently, the number of heartbeats in most cases returns to the usual values for the patient (in the first hours or days). Even for the uncomplicated course of myocardial infarction, there are various arrhythmias (most often extrasystoles). Many violations of the heart rhythm occur without subjective sensations. They can arise and terminate imperceptibly for the patient. They can be considered not as a complication of myocardial infarction, but as characteristic symptoms of myocardial infarction.
Arterial pressure in the first hours of the disease at the height of the pain syndrome is often increased. In the future, it returns to the usual level for the patient, or, more often, somewhat decreases (mainly due to systolic). With uncoupled pain syndrome, cardiogenic shock can develop.
The size of the heart in uncomplicated flow often does not change. Heart enlargement is usually observed with complications such as interventricular septum and papillomavirus ruptures, heart aneurysms, left ventricular dilation. The enlargement of the heart can also be due to the presence of arterial hypertension, atherosclerotic and post-infarction cardiosclerosis, and the like.
When palpation of the heart area in patients with both transmural and nontransmural myocardial infarction, atrial pulsation, an increase in the zone of apical shock, and a paradoxical pulsation to the left of the sternum are often detected.
With an auscultatory study, in the first few hours from the development of myocardial infarction, weakened I tone, so that the II tone is heard as loud. With a vast heart attack, deaf tones are heard. Perhaps the appearance of systolic murmur over the tip, which is usually regarded as a poor prognostic sign.
A silent systolic murmur over the apex, which occurs on the second and subsequent days, is regarded as a sign of relative insufficiency of the bivalve valve when the left ventricle expands or the papillary muscle of the left ventricle is damaged. Approximately 25% of patients listen to the rhythm of the canter. Atrial canter (IV tone) is more common than ventricular (III tone). Sometimes III and IV additional tones merge (summation canter). Ventricle canal is more often observed with left ventricular failure with or without enlargement of the heart. The atrial can be listened to without heart failure. The canter rhythm most often appears on the first or second day and stops when the heart activity improves. With a fairly extensive infarction of the anterior wall of the left ventricle, short-term pericardial noise can be heard in a restricted area.
For large-heart attack myocardial infarction is characterized by a rise in temperature to 38 ° C in the first days after the development of myocardial infarction. This increase in temperature is due to the development of resorption-necrotic syndrome.
Aseptic necrosis of the myocardium is also accompanied by changes in the morphological pattern of blood (leukocytosis) and acceleration of erythrocyte sedimentation. The temperature reaction lasts a few days and stops for a week. The rise in temperature can be caused not only by necrotic changes in the heart muscle, but also by pericarditis, parietal endocarditis, and complications from other organs and systems. Myocardial infarction, especially shallow foci, can occur against a background of normal temperature.
Arrhythmic variant and symptoms of myocardial infarction
Violations of the heart rate are to some extent present in almost all patients with myocardial infarction. Their presence is not a basis for diagnosing an arrhythmic variant of myocardial infarction. For the arrhythmic variant of myocardial infarction, the prevalence of cardiac rhythm disturbances and accompanying symptoms is characteristic.
At the heart of the development of rhythm disturbances in myocardial infarction is the electrical instability of the heart, which developed as a result of a violation of the process of cardiac muscle metabolism, microcirculation and shifts in the water-electrolyte state.
As a rule, the arrhythmic variant proceeds in the form of paroxysms of gastric or supraventricular tachycardia, periods of ventricular fibrillation, ciliary tachyarrhythmia, transverse blockade or high-grade atrioventricular block with bradysystole. The pain may not be expressed or go away after the heart rhythm is broken.
With this option, often arrhythmogenic cardiogenic shock develops, mortality is high.
The arrhythmic variant can lead to a significant deterioration in the blood supply and ischemia of the brain. Often such a symptomatology is regarded as a cerebral variant of a myocardial infarction (for example, with the Morgagni-Adams-Stokes syndrome). But in this case, cerebral symptoms should be regarded as symptoms of myocardial infarction of the arrhythmic variant.
Despite the fact that in the arrhythmic variant, rhythm disturbances first come to the fore, then the general patterns of development and course of myocardial infarction are repeated.
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The asthmatic variant (status asthmaticus) is manifested by an attack of suffocation as a result of the development of acute left ventricular failure. The patient complains of shortness of breath, a feeling of lack of air (a picture of cardiac asthma). The pain syndrome at the same time goes to the second plan or is completely absent. The absence of pain can be caused by the appearance of foci of necrosis in a zone poor in the receptor apparatus.
This variant often develops with repeated myocardial infarctions, chronic left ventricular aneurysm, and infarction of papillary muscles. The asthmatic variant of myocardial infarction is characterized by considerable severity and high mortality.
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Gastralgic variant and symptoms of myocardial infarction (status abdominalis)
This variant of myocardial infarction "simulates" the clinic of an acute abdomen or acute gastritis. It is characterized by a combination of pain in the upper floor of the abdominal cavity with various kinds of dyspeptic disorders. Patients may experience abdominal wall tension, bloating, nausea, vomiting, hiccough, acute atony of the stomach, intestinal paresis. A painful process can begin with vomiting, pain in the pit of the stomach, sometimes diarrhea joins.
At objective research the high standing of the diaphragm, the increase in the Traube area, pronounced tympanitis in the region of the stomach, the absence of peristalsis, the noise of splashing in the stomach are noted. In a number of cases, atony of the stomach is complicated by the development of acute gastric ulcers and the occurrence of gastrointestinal bleeding.
The development of pain in the upper abdomen is most likely due to the spread of painful impulses in a number of underlying parts of the posterior horns of the spinal cord. Most often, this clinical variant is observed with lower myocardial infarction. Sometimes a similar clinic is caused by a combination of myocardial infarction with acute pancreatitis.
It occurs relatively rarely, more often in elderly patients with severe generalized atherosclerosis. In the clinical picture, the symptoms of transient cerebral circulation disorders predominate. Most often cerebrovascular variant of myocardial infarction is manifested by syncope, nausea, vomiting, focal neurological symptoms. Pain in the heart of such patients, as a rule, poorly expressed or completely absent. Disorders of cerebral circulation are associated with a decrease in cardiac output, leading to hypoxia and cerebral edema.
With thrombosis and embolism of cerebral vessels, a picture of acute disturbance of cerebral circulation develops, which does not present any special diagnostic difficulties.
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Sometimes myocardial infarction can occur asymptomatically or with minimal manifestations of heart muscle damage. The patient does not pay attention to unexpressed dyspnea, small pains in the area of the heart, or to an increase in their occurrence. Probably, such a course is caused by reduced sensitivity of the nervous system, a number of constitutional factors, peculiarities of coronary circulation disturbance and metabolism in the cardiac muscle. Asymptomatic myocardial infarction should be distinguished from painless, since although pain is absent in both forms, but with asymptomatic there are no other symptoms (disturbances of heart rhythm, blood circulation, etc.).
The incidence of cases of painless forms of myocardial infarction is from 4 to 25% of all cases of myocardial infarction.
Such forms of myocardial infarction are most often diagnosed accidentally when they are being treated for another disease.
The painful variant is regarded by most authors as a typical course of myocardial infarction. The remaining forms (asthmatic, arrhythmic, cerebrovascular and abdominal variants) are referred to as atypical course of myocardial infarction. Atypical variants (except asymptomatic) can not be attributed to uncomplicated forms of myocardial infarction.
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